The physiological role of pain-induced dopamine release within the nucleus accumbens in affections
| Project/Area Number |
26460330
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
General pharmacology
|
|---|
| Research Institution | Tokyo Metropolitan Institute of Medical Science (2015-2016)
Hokkaido University (2014) |
|---|
Principal Investigator |
IDE Soichiro 公益財団法人東京都医学総合研究所, 精神行動医学研究分野, 主席研究員 (30389118)
|
|---|
| Project Period (FY) |
2014-04-01 – 2017-03-31
|
| Project Status |
Completed (Fiscal Year 2016)
|
| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
|---|
| Keywords | 側坐核 / ドパミン / 痛み / 報酬 / うつ / 負情動 / 嫌悪 / 薬理学 / 情動 |
|---|
| Outline of Final Research Achievements |
In the present study, we examined the physiological role of pain-induced dopamine release within the nucleus accumbens in pain-induced aversion. A significant increase in the dopamine level and increased neuronal activity within the rostral part of the nucleus accumbens shell were caused by the acetic acid intraperitoneal injection. The conditioned place aversion (CPA) induced by the acetic acid intraperitoneal injection was abolished in dopamine transporter knockout mice. Further, reward-induced dopamine release in the nucleus accumbens of neuropathic pain rats were investigated. Pain relief and sucrose solution were given to the neuropathic pain rats as rewards. Rewards increased dopamine release in the early, but not late, phase of pain. Dysfunction of the mesolimbic dopamine reward circuit might be a common neuronal mechanism underlying chronic pain and depression and a potential target to develop novel analgesic and antidepressant medications.
|
Report
(4 results)
Research Products
(15 results)
-
-
[Journal Article] Loss of GluN2D subunit results in social recognition deficit, social stress, 5-HT2C receptor dysfunction, and anhedonia in mice.2017
Author(s)
Yamamoto H, Kamegaya E, Hagino Y, Takamatsu Y, Sawada W, Matsuzawa M, Ide S, Yamamoto T, Mishina M, Ikeda K
-
Journal Title
Neuropharmacology
Volume: 112(Pt A)
Pages: 188-197
DOI
Related Report
Peer Reviewed / Open Access
-
-
-
-
-
-
-
-
-
-
-
-
-
